Primary and secondary insomnia factors affecting insomnia explanations of other sleep disorders



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DISORDERS OF SLEEP


To read up on sleep disorders, refer to pages 61–70 of Eysenck’s A2 Level Psychology.

Ask yourself

  • What are the explanations of insomnia?

  • What causes sleepwalking?

  • What is narcolepsy?


What you need to know

PRIMARY AND SECONDARY INSOMNIA

FACTORS AFFECTING INSOMNIA

EXPLANATIONS OF OTHER SLEEP DISORDERS

  • Distinguish between primary and secondary insomnia and their causes

  • Consider factors such as sleep hygiene, stress, environmental factors, and illness that affect insomnia

  • Consider the nature and causes of somnambulism and narcolepsy


PRIMARY AND SECONDARY INSOMNIA

Insomnia is the condition in which there are problems falling asleep and/or staying asleep, and the sleep that occurs tends not to be deep and is easily disturbed. Insomnia is also, unsurprisingly, linked with fatigue, having poor attention, impaired judgement, decreased performance, being irritable, and an increased risk of accidents. Insomnia is not a single condition as there are different forms based on the degrees of severity (mild, moderate, severe, acute, chronic) and the causes of the insomnia.

Insomnia can be categorised as primary or secondary insomnia depending on the cause. Primary insomnia is the most common form of insomnia and has no clear underlying cause. There is a sleep problem, but there is no physiological or psychiatric cause, and it is likely that the sleep problem is the result of maladaptive behaviours or learning. The clinical characteristics are that the individual has suffered from insomnia for at least a month but this would not be linked with any other sleep disorder, such as parasomnia or narcolepsy, nor with another psychopathology such as clinical depression, nor with medications or substance abuse. Worrying about the insomnia can lead to a cycle that is hard to break because the more a person focuses on their sleep problems the less likely they are to get good quality sleep.

Secondary insomnia is insomnia that has a specific cause. Examples of such causes include sleep apnoea, restless legs syndrome (RLS), circadian rhythm disorders due to night shiftwork, and various medical, substance use, and emotional problems.



FACTORS AFFECTING INSOMNIA

These factors affect insomnia because they interfere with the natural progression of brain activity from daytime functioning to slowing down to sleeping. This progression was described earlier as part of the sleep–wake cycle.



Environmental Factors

Stimuli such as bright lights, loud noises, very hot or very cold rooms, an uncomfortable bed, or a snoring companion can all contribute to insomnia because they interfere with the brain’s natural calming down of neural activity. A change in the location where one sleeps, can also boost brain activity and lead to insomnia, hence we often do not sleep well unless in our own bed!



Stress

Acute stress, perhaps from a major life event such as an exam or a job change, can lead to insomnia, again because brain activity is heightened, the sympathetic ANS is active, and so the parasympathetic ANS cannot switch. Acute stress is transitory and so when it is over normal sleep should resume. However, with chronic stress the stressor persists, and so sympathetic ANS activity remains high, which can lead to long-term disrupted sleep.



Sleep Hygiene/Bedtime Behaviour

Sleep hygiene refers to the habits and bedtime behaviour patterns that promote the calming and slowing down of the brain in preparation for sleep. Poor sleep hygiene refers to habits that do not promote this progression: consuming caffeine or alcohol or taking in nicotine interfere with brain activity and the sleep process. Similarly stimulating activities, particularly if these take place in the bedroom, such as watching TV, chatting on the phone, or doing homework can also lead to insomnia. A delayed bedtime for whatever reason—more stories, more TV, a drink—also delays settling down ready for sleep. Night fears, e.g. of the dark, also prevent the calming down needed for sleep. Poor sleep hygiene means the brain is very active, it is still alert and in daytime mode, and so the parasympathetic ANS (autonomic nervous system), the rest-and-digest mechanism, will not switch on and calm the brain, and insomnia is the result. Taking naps during the day is another aspect of sleep hygiene that can perpetuate insomnia.



Sleep apnoea

There are two types of apnoea, obstructive and central. The main characteristic of obstructive sleep apnoea is fairly brief interruptions of breathing when asleep, each interruption being followed by choking and gasping as the sufferer struggles for air. The sufferer often snores loudly. This happens because the upper airways temporarily collapse during sleep so that air cannot get into or out of the lungs. Blood oxygen levels may drop, and each episode ends with awakening to some extent and then going back to sleep. Though children and normal weight people can suffer from sleep apnoea, possibly because of a smaller than usual upper airway, it is more common in overweight, middle-aged people, more often in men than in women.

Obstructive sleep apnoea (OSA) is linked to impaired cognition. Macey et al.’s (2002, see A2 Level Psychology page 64) MRI scanning study showed small but significant reductions in brain neurons, presumably because of oxygen deprivation. Kumar et al. (2008, see A2 Level Psychology page 64) also used MRI scans to show that there is measurable loss of nearly 20% of the brain tissue in the mammillary bodies that are part of the memory circuits. Childhood OSA is also linked to poor behaviour, growth, attention, memory and classroom performance, and lower childhood IQ scores. The effects of OSA on cardiovascular health have been studied in children aged 12 to 26 months (Goldbart et al., 2007, see A2 Level Psychology page 65) and children with OSA, unlike matched controls, showed high levels of ventricular heart strain. Both the inflammation and signs of heart strain reduced to normal levels following surgery removing the adenoids.

Central sleep apnoea presents as periods of not breathing when asleep but the cause here is organic. The brain does not send the necessary normal signals to the breathing muscles, the diaphragm and the intercostals, so they do not contract frequently enough and so the individual does not take a breath often enough. It is the central control mechanism in the brainstem that is faulty, sometimes because of a stroke, but oxygen therapy can produce significant improvements in patients (White, 2005, see A2 Level Psychology page 65).



Personality

Stress is clearly linked to insomnia. Vgontzas et al. (2001, see A2 Level Psychology page 65) found high levels of stress hormones in insomniacs and concluded that insomniacs suffer from hyperarousal in the central nervous system (CNS) caused by chronic activation of the hypothalamic–pituitary–adrenal axis leading to increased risk of chronic anxiety and depression and physiological damage. De Sainte Hilaire, Straub, and Pelissolo (2005, see A2 Level Psychology page 66) hypothesised that serotonin activity could relate to both temperament and insomnia. They found harm avoidance correlated positively with sleep latency, the time taken to go from waking into deep sleep. Research by Leblanc et al. (2007, see A2 Level Psychology page 66) found strong links between insomnia and high scores on depression, anxiety, neuroticism, extraversion, arousal predisposition, stress perception, and emotion-oriented coping. Similar links were found by Soehner, Kennedy, and Monk (2007, see A2 Level Psychology page 66) using the Eysenck Personality Inventory for extraversion and neuroticism, the Pittsburg Sleep Quality Index for quality of sleep, and the Sleep Timing Questionnaire for the duration, timing, and latency of sleep. They found links between higher neuroticism as a personality trait and the timing and poorer quality of sleep but not with sleep duration.



Deadly Insomnia

There are very rare cases in which insomnia becomes not just pathological but deadly. This has been identified as a genetic condition named as fatal familial insomnia (FFI). It seems to have started with a mutation affecting certain proteins in the brain, particularly in the thalamus, so that they mis-fold and form prions. These prions clump together, cause neuron deaths, and the area of the brain affected develops a sponge-like structure, full of holes. Death follows, usually within a year of the first signs of the disorder developing.



EVALUATION

  • Sample bias. The problem with research into obstructive sleep apnoea (OSA) is that the sample size is small, especially as the frequency of OSA in the Western world is only 5%. This means that there will always be methodological issues with interpreting the data and generalising it to the population of those with the disorder.

  • Direction of effect. The problem with research into the factors affecting insomnia is that it is mainly correlational and so we cannot be sure of the direction of effect. Thus, rather than high stress hormone levels and CNS activity causing insomnia, it could be suggested that insomnia is causing the stress and arousal. Similarly, rather than day-time napping causing insomnia, the insomnia may be causing the day-time napping. In fact these relationships are likely to be two-directional, in that both the factors and the insomnia influence each other.

  • Cause and effect. As the research into the factors is correlational it does not establish cause and effect. Thus, we cannot say that the factors cause insomnia only that they are linked, which limits the conclusions that can be made.

  • Reductionism of correlations. Correlations are oversimplified because they only examine two variables when there may be other factors that affect the insomnia.

  • Using normal samples instead of insomniacs. The participants in Soehner et al.’s (2007) study into personality were not insomniacs but normal working adults, which limits what the study can tell us about insomnia!

  • Self-report criticisms. The questionnaires in Soehner et al.’s (2007) study were all self-report, mail-in ones. The anonymity of the questionnaire can encourage greater accuracy of answers, and so internal validity (truth). However self-report is also subject to participant reactivity, which reduces internal validity because participants may have been influenced by what they supposed the researchers were looking for (demand characteristics) or by what they felt was socially desirable or even perhaps macho.


EXPLANATIONS OF OTHER SLEEP DISORDERS

Sleepwalking

Somnambulism (sleepwalking) is a relatively common sleep disorder, with estimates that it affects about one in ten of us at some point in our lives. Typically the eyes are open, though often described as glazed or staring in appearance. Somnambulism is most likely to occur during NREM stages 3 and 4, in slow-wave sleep. It can occur in REM sleep but this is much less likely. NREM sleep is earlier in the sleep period and so episodes of somnambulism tend to be in the earlier rather than later parts of the night. Somnambulism is most common in childhood, peaking just before or at the time of puberty, however it can continue into adulthood. An episode may last only a few seconds, but can last hours, and when awake the individual will have no memory of what they have been doing. The causes of somnambulism include a genetic predisposition, fatigue, previous lack of sleep, stress, or anxiety. In adults, alcohol and other drugs seem to act as triggers.

The genetic element in somnambulism is supported by Hublin et al. (1997, see A2 Level Psychology page 67) who used the Finnish twin cohort and found that the genetic contribution to somnambulism in childhood was 66% in men and 57% in women, and for adult somnambulism was 80% in men and 36% in women. The sex difference in childhood somnambulism does not seem significant, but it is puzzling why there is such a major difference between the sexes in adult somnambulism. Szelenberger, Niemcewicz, and Dabrowska (2005, see A2 Level Psychology page 67) offer an explanation of sleepwalking as they found both low and declining levels of delta waves that could be signs of a chronic inability to sustain slow-wave sleep. The main issue with somnambulism, apart from the anxieties it may cause, is the moderately high risk of somnambulists injuring themselves during an episode—in some cases bones have been broken!

Narcolepsy

Narcolepsy is rare but is characterised by chronic sleepiness, and so the individual may fall asleep at any time. Short naps of 10 to 20 minutes are common, after which the sleepy feeling is temporarily reduced, only to reappear with 2 to 3 hours. Cataplexy can also occur. This is when the muscles lose strength when strong emotions are experienced. The body may droop, sag, or even collapse as if paralysed, but there is no loss of consciousness, the individual does not faint. The episodes may be over within seconds or last some minutes. Sleep paralysis can also occur either at the beginning of sleep or when first awakening and is a brief loss of the ability to move, apart from the breathing muscles and eye muscles. This usually lasts a few minutes and can be very distressing, especially as it is sometimes accompanied by a sense of fear or dread, e.g. the individual thinking they are dead, and even hallucinations. Sleep hallucinations also may occur when dropping off to sleep or when awakening.

Research has established that in non-human animals, such as dogs and mice, a genetic mutation can cause narcolepsy. Mignot discovered that in dogs this mutation also produced a deficiency in a receptor for the neurotransmitter hypocretin, which blocks communication between neurones, particularly messages relating to when the body should wake. Injections of hypocretin in dogs reversed their narcolepsy, but this could not be generalised to humans as the human disorder has environmental as well as genetic causes, it is a nature and nurture phenomenom. Evidence for a genetic basis is provided by Mignot’s (1998) twin study. This showed a MZ 25–31% concordance rate for human narcolepsy and 1–2% for first-degree relatives of narcoleptics, which compares to a very low rate in the general population. A hypocretin (or orexin as it is also known) deficiency is definitely implicated in human narcolepsy, as Thannickal et al. (2000, see A2 Level Psychology page 68) found that narcoleptics have a reduction of about 85–95% in hypocretin neurons, whilst melatonin neuron numbers are unaffected, with the hypocretin loss being degenerative and perhaps autoimmune. Research in South China showed that narcolepsy is more common in those born in winter. We cannot be sure what it is about winter but one possibility is that viruses are more common in winter, so there might be a viral interaction with genes. Kim et al.’s (2008, see A2 Level Psychology page 69) research showed an increase in GABA levels in the medial prefrontal cortex of narcoleptics. However this may be an effect rather than a cause, and cause and effect cannot be established from correlational data. Certainly it seems most likely that narcolepsy is multi-factorial and so can only be explained by an interaction of multiple factors, maladaptive HLA genes, environmental factors, degenerative neurological changes, and abnormal neurotransmitter levels.

SO WHAT DOES THIS MEAN?

Insomnia is complex because it is not one condition. There may be a clear cause, as in secondary insomnia, or there may be no obvious cause, as in primary insomnia. Whichever the type, stress and anxiety about the insomnia can perpetuate the condition. There are also a number of factors that seem to explain insomnia, such as stress, personality, and sleep hygiene, to name but a few. However, these factors are only correlated and so we cannot conclude that they cause insomnia. In fact, any relationships between the factors in insomnia may not be linear, instead they may be bi-directional where the factors influence insomnia and insomnia influences the factors. For example, insomnia is linked to an anxious, neurotic type of personality, which means the anxious personality may influence insomnia, however, the insomnia may increase the anxiety. Thus, conclusions about the factors are limited to associations only rather than causal effects.



Insomnia is not the only sleep disorder as sleepwalking and narcolepsy are two further sleep disorders. There seems to be a genetic basis to these conditions but nurture also influences them. For example, such can affect sleepwalking and narcolepsy is linked to being born in the winter.

Over to you

1. Outline explanations of primary and secondary insomnia. (9 marks)
2. Discuss the factors affecting insomnia. (25 marks)
3. Describe explanations of other sleep disorders. (9 marks)

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